Up to 30% of people with psoriasis develop psoriatic arthritis, and nobody can yet say which ones. This review argues the plaque is not just an inflamed patch of skin but a source of immune cells that reach the joint: T cell clones and myeloid precursors shared between skin and synovium. But arrival alone does not cause arthritis. What decides it is the stromal niche, in particular synovial fibroblasts, which act as gatekeepers.
Fatigue affects 35–82% of patients with musculoskeletal disease and roughly one in two reports it as severe — yet it correlates poorly with CRP, DAS28 and even MRI-detected synovitis. This review covers what fatigue is, how to measure it, the biology proposed to explain it, why remission so often fails to resolve it, and what actually works: biologics, exercise, CBT and the EULAR non-pharmacological recommendations.
Antimicrobial peptides are innate defence molecules — but in RA they become autoantigens, immune adjuvants and drivers of bone erosion. This review tracks LL-37, the defensins and the S100 proteins across five stages, from mucosal predisposition through to chronic synovitis, and makes the case that they amplify rather than initiate disease. Calprotectin already outperforms CRP and ESR for reflecting joint inflammation, yet no AMP-based agent has entered an RA trial since a phase II failure in 2019.
Sex differences in rheumatic disease are usually pinned on oestrogen, but this review argues the picture is far more tangled. Oestradiol drives disease in SLE while appearing protective in Sjögren’s and RA; X chromosome dosage raises risk independently of hormones — triple X carries a 2.9-fold higher Sjögren’s prevalence; and gut bacteria reactivate oestrogen through β-glucuronidase, closing a loop between all three mechanisms.
In a UCL cohort of prolonged SACQ lupus patients — elevated anti-dsDNA and/or low C3 for 6+ months with no clinical activity — 63% flared over a mean 3.3 years. Rising IgG anti-dsDNA and falling C3 at one visit independently predicted flare and sustained activity at the next, including moderate-to-severe disease, in a visit-by-visit longitudinal model. The risk from low C3 rose sharply below 0.9 g/L and flattened above it.
IgA vasculitis and IgA nephropathy share HLA susceptibility, 21 GWAS risk loci, elevated Gd-IgA1 and renal biopsies that cannot be told apart — yet IgAN now has five approved therapies and IgAV has none, because IgAV patients were excluded from every trial that delivered them. What changes today: KDIGO 2025 lowers the treatment threshold to 0.5 g/day of proteinuria, and it explicitly covers IgA vasculitis.
Relapsing polychondritis is not one disease with variable severity. A French cohort splits it into three clusters whose mortality runs 4%, 13% and 58% — and the worst cluster is almost certainly VEXAS, which this review argues should be treated as a disease mimic rather than a subtype. Chondritis is absent at presentation in 40%, there is no confirmatory test, and no randomised trial has ever been conducted.
ACPA-positive and ACPA-negative RA take the same total time from first symptom to arthritis — but split it in mirror image. Seropositive patients reach the rheumatologist later and convert faster; seronegative patients arrive sooner and linger, leaving roughly twice as long an actionable window once they are in front of you. Each entity carries its own signature before arthritis exists.
A 2026 narrative review arguing that B cells are the single through-line of Sjögren disease — connecting autoantibodies, glandular pathology, the highest lymphoma risk of any autoimmune disease, and the emerging drug pipeline. Endotyping by B-cell activity may identify who develops lymphoma and who responds to B-cell-targeted therapy, as newer BAFF/APRIL, CD40L, BTK and FcRn agents succeed where rituximab failed.
A 2026 review of renal involvement in systemic sclerosis — a spectrum well beyond scleroderma renal crisis (SRC), covering the diagnostic constellation, five converging mechanisms, risk factors (anti-RNA polymerase III, early dcSSc, steroids), and the management essentials: immediate ACE inhibition, never stopped for a rising creatinine.